August 7, 2019Cardiovascular Research
Therapeutic inhibition of microRNA-34a ameliorates aortic valve calcification via modulation of Notch1-Runx2 signalling
Key result
Inhibition of miR-34a suppressed aortic velocity, calcium deposition of aortic valves, and cardiac hypertrophy in a CAVS mouse model via the Notch1-Runx2 signalling pathway.
Why the study?
Calcific aortic valve stenosis is the most common valvular heart disease and increases with aging, but effective pharmacological therapies remain unestablished.
Does locked nucleic acid miR-34a inhibitor reduce aortic valve calcification in preclinical models of CAVS?
Population
Human aortic valve tissue from CAVS and AR patients, porcine AVICs, and wire injury CAVS mice
Comparison
Inhibition or overexpression of miR-34a vs controls
Design
Preclinical translational and animal model study
Authors
Discussion
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Member takes
Implication
miR-34a inhibition attenuates CAVS in mice; hypothesis-generating for human translation.
Structured PICO
Does locked nucleic acid miR-34a inhibitor reduce aortic valve calcification in preclinical models of CAVS?
P
Population
Human aortic valve tissue from patients with CAVS or AR, porcine AVICs, and a wire injury CAVS mouse model.
I
Intervention
Locked nucleic acid miR-34a inhibitor
C
Comparator
miR-control
O
Outcome
Aortic valve calcification and Notch1-Runx2 signalling expressionsurrogate
Therapeutic inhibition of miR-34a ameliorates aortic valve calcification via the Notch1-Runx2 signalling pathway in preclinical models, suggesting a potential novel therapeutic target for CAVS.
Cite This Study
Toshima et al. (2019) studied Calcific aortic valve stenosis (CAVS). miR-34a inhibitor vs. miR-control / AR patients was evaluated on Aortic valve calcification, Notch1-Runx2 signalling, aortic velocity, and cardiac hypertrophy. Inhibition of miR-34a suppressed aortic velocity, calcium deposition of aortic valves, and cardiac hypertrophy in a CAVS mouse model via the Notch1-Runx2 signalling pathway.